Decrease of LFA-1 Is Associated with Upregulation of TGF-β in CD4+T Cell Clones Derived from Rats Nasally Tolerized against Experimental Autoimmune Myasthenia Gravis

Clinical immunology and immunopathology Pub Date : 1998-12-01 DOI:10.1006/clin.1998.4537

Bao-Guo Xiao , Guang-Xian Zhang, Fu-Dong Shi, Cun-Gen Ma, Hans Link

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引用次数: 10

Abstract

Tolerance to experimental autoimmune myasthenia gravis by nasal administration of microgram amounts of acetylcholine receptor (AChR) has been reported. To elucidate the mechanisms behind tolerance induction via the respiratory tract and the involvement of CD4⁺T cells, we established AChR-specific CD4⁺CD8⁻T cell clones from nasally tolerized rats. Nasal tolerance decreased leukocyte function-associated antigen-1 (LFA-1) expression in CD4⁺T cells from tolerized rats. There was no difference between nasally tolerized and control rats in expression of intercellular adhesion molecule-1. The levels of transforming growth factor-β (TGF-β) mRNA-expressing cells were upregulated in CD4⁺T cell clones after tolerance induction. These findings suggest that decreased LFA-1 expression in CD4⁺T cells contributes to reduction of the infiltration of inflammatory CD4⁺T cells, while upregulated TGF-β may inhibit lymphocyte functions.

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实验性自身免疫性重症肌无力鼻耐受大鼠CD4+T细胞克隆中LFA-1的降低与TGF-β的上调相关

经鼻给药微量乙酰胆碱受体(AChR)对实验性自身免疫性重症肌无力的耐受性已有报道。为了阐明通过呼吸道诱导耐受性和CD4+T细胞参与的机制，我们从鼻耐受大鼠中建立了achr特异性CD4+CD8−T细胞克隆。鼻腔耐受降低了耐受大鼠CD4+T细胞中白细胞功能相关抗原-1 (LFA-1)的表达。鼻耐受大鼠与对照组细胞间粘附分子-1的表达无差异。CD4+T细胞克隆耐受诱导后，表达TGF-β mrna的细胞水平上调。上述结果提示，CD4+T细胞中LFA-1表达的降低有助于减少炎性CD4+T细胞的浸润，而TGF-β的上调可能抑制淋巴细胞功能。

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Clinical immunology and immunopathology

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